Increased Levels of the Soluble Variant of the Vascular Endothelial Growth Factor Receptor VEGFR-1 Are Associated with a Poor Prognosis in Wound Healing

Eming, Sabine A.; Lauer, Gereon; Cole, Melanie; Jurk, Sandra; Christ, Hildegard; Hornig, Carsten; Krieg, Thomas; Weich, Herbert A.

doi:10.1111/j.0022-202x.2004.23310.x

Cited by 30 publications

(18 citation statements)

References 20 publications

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“…This is in agreement with a previous experimental study that demonstrated decreased VEGF‐R1 following wounding28. In contrast, non‐healing wounds have an excess of soluble VEGF‐R1, a naturally occurring inhibitor of VEGF, which may explain the relative lack of angiogenic response in these wounds29.…”

Section: Discussionmentioning

confidence: 99%

Angiogenesis, vascular endothelial growth factor and its receptors in human surgical wounds

Kumar

Staton

Cross

et al. 2009

British Journal of Surgery

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Section: Discussionmentioning

confidence: 99%

Angiogenesis, vascular endothelial growth factor and its receptors in human surgical wounds

Kumar

Staton

Cross

et al. 2009

British Journal of Surgery

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“…In preeclampsia, various studies have shown that hypoxia, oxidative stress, and an excess of VEGF-A in the endometrium regulate the production of sVEGFR1 [100,104,105]. Moreover, increased expression of sVEGFR1 was observed in patients with wound healing defects [106], as well as in patients with idiopathic pulmonary arterial hypertension [107] or adult respiratory distress syndrome [108]. Both pathologies are associated with abnormal vascular permeability.…”

Section: Alternative Splicing Of Vegfr1: From Anti-angiogenic To Pmentioning

confidence: 99%

Splice Variants of the RTK Family: Their Role in Tumour Progression and Response to Targeted Therapy

Abou-Faycal

Hatat

Gazzéri

et al. 2017

IJMS

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Receptor tyrosine kinases (RTKs) belong to a family of transmembrane receptors that display tyrosine kinase activity and trigger the activation of downstream signalling pathways mainly involved in cell proliferation and survival. RTK amplification or somatic mutations leading to their constitutive activation and oncogenic properties have been reported in various tumour types. Numerous RTK-targeted therapies have been developed to counteract this hyperactivation. Alternative splicing of pre-mRNA has recently emerged as an important contributor to cancer development and tumour maintenance. Interestingly, RTKs are alternatively spliced. However, the biological functions of RTK splice variants, as well as the upstream signals that control their expression in tumours, remain to be understood. More importantly, it remains to be determined whether, and how, these splicing events may affect the response of tumour cells to RTK-targeted therapies, and inversely, whether these therapies may impact these splicing events. In this review, we will discuss the role of alternative splicing of RTKs in tumour progression and response to therapies, with a special focus on two major RTKs that control proliferation, survival, and angiogenesis, namely, epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor-1 (VEGFR1).

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“…44 Additional disruption of VEGF signaling in chronic wounds may come from an increase in soluble VEGFR-1 observed in venous ulcers. 45 Importantly, exogenous VEGF has been successfully used in animal studies 46 and proposed for use in treatment of chronic wounds in humans.…”

Section: Vascular Endothelial Growth Factormentioning

confidence: 99%

Acute and Impaired Wound Healing

Demidova-Rice

Hamblin

Herman

2012

Advances in Skin &Amp; Wound Care

172

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Increased Levels of the Soluble Variant of the Vascular Endothelial Growth Factor Receptor VEGFR-1 Are Associated with a Poor Prognosis in Wound Healing

Cited by 30 publications

References 20 publications

Angiogenesis, vascular endothelial growth factor and its receptors in human surgical wounds

Angiogenesis, vascular endothelial growth factor and its receptors in human surgical wounds

Splice Variants of the RTK Family: Their Role in Tumour Progression and Response to Targeted Therapy

Acute and Impaired Wound Healing

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